title: Coronary artery disease from isolated non-H2-determined incompatibilities in transplanted mouse hearts.
abstract: BACKGROUND
  Most studies of vascular disease in transplanted organs have used combinations involving disparities determined by genes of the major histocompatibility complex (MHC). This report describes examples of coronary vascular disease occurring in transplanted mouse hearts involving isolated, non-H2-determined incompatibilities.
  
  
  METHODS
  Mice, incompatible in respect of HY, H4, or H60, were selected. For H60, the incompatibility depended on breeding congenic pairs or the introduction of H60 by transgenic methods because the latter method results in more widespread expression. Transplant survival was determined, and the appearance and prevalence of coronary artery vasculopathy (CAV) was established by appropriate histologic methods.
  
  
  RESULTS
  Advanced changes of CAV were found at 56 days in transplants involving incompatibilities confined to HY or H4. In both combinations, skin grafts were also rejected. H60 incompatibility does not result in skin graft rejection and only a minority of heart transplants shows evidence of CAV. If heart transplants are preceded by skin grafts bearing both H60 and HY incompatibilities to promote "help" in generating immunity, H60 incompatible hearts develop advanced CAV. Heart transplants in all non-MHC categories ostensibly survive in excellent condition throughout this period despite their CAV.
  
  
  CONCLUSIONS
  CAV can develop as a consequence of non-MHC incompatibilities alone and even when antigens are sparsely expressed on cardiac tissue. Presensitization leads to much more severe vascular disease. Human leukocyte antigen compatible kidney transplants may also develop vascular disease and patients manifesting reactivity to MHC antigens should also be more prone to develop vascular disease because of undetectable non-MHC incompatibilities.
authors.affiliation: Department of Surgery, Harvard Medical School, Massachusetts General Hospital, Boston, MA 02114, USA. psrussell@partners.org
authors.forename: Paul S
authors.initials: PS
authors.lastname: Russell
authors.forename: Catharine M
authors.initials: CM
authors.lastname: Chase
authors.forename: Joren C
authors.initials: JC
authors.lastname: Madsen
authors.forename: Tsutomu
authors.initials: T
authors.lastname: Hirohashi
authors.forename: Lynn D
authors.initials: LD
authors.lastname: Cornell
authors.forename: Thomas J
authors.initials: TJ
authors.lastname: Sproule
authors.forename: Robert B
authors.initials: RB
authors.lastname: Colvin
authors.forename: Derry C
authors.initials: DC
authors.lastname: Roopenian
mesh_terms: D000818:Animals; D003324:Coronary Artery Disease / Q000276:immunology* / Q000473:pathology; D005260:Female; D006084:Graft Rejection / Q000276:immunology; D006085:Graft Survival; D006182:H-Y Antigen / Q000276:immunology; D016027:Heart Transplantation / Q000276:immunology*; D006648:Histocompatibility; D008297:Male; D051379:Mice; D020297:Mice, Congenic; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic; D015778:Minor Histocompatibility Antigens / Q000235:genetics / Q000276:immunology*; D016038:Skin Transplantation / Q000276:immunology; D013997:Time Factors
chemical_list: D006182:H-Y Antigen; D015778:Minor Histocompatibility Antigens; C114735:minor H antigen H60